Figure 10. Attenuation of lung injury following blast limb trauma by NaHS treatment.

Blast limb trauma induces systemic inflammatory response, oxidative stress and suppression of CSE/H₂S pathway. All those induce to the disruption of endothelium and the increase of permeability of gas blood barrier, and ultimately lead to lung oedema formation and remote lung injury following blast limb trauma. Exogenous NaHS treatment attenuates lung injury following blast limb trauma via preventing the decrease of plasma H₂S, suppressing the production of cytokines and adhesion molecular, such as TNF-α, IL-6, IL-10, ICAM1, CXCL-2 and CD11b [31] and ameliorating oxidative stress though Nrf2, K⁺ _ATP and Cl⁻ channel and inhibition of iNOS/NO pathway and L-type Ca2+ channels [44], [45], [46].